Acetic acid, also known as ethanoic acid, ethylic acid, and methane carboxylic acid, is a mild chelating agent. Solutions diluted to less than 40% concentrations, such as table vinegar and hair-wave neutralizing products, are usually harmless, but if used inappropriately they may cause injuries. Chemical exposures may cause symptoms of upper- and lower-airway irritation, including cough, tachypnea, wheezing, nose and throat irritation, and pharyngeal and pulmonary edema. Other symptoms found are tooth erosion, conjunctivitis, headache, nausea, vomiting, impaired vision, abdominal pain, eye pain, and whitish discoloration of the skin. In such cases, initial treatment involves irrigation.

Carbolic acid is a hydrocarbon derived from coal tar, which acts to cause damage secondary to its ability to induce denaturation and necrosis. ^, The most common adverse effects are dermatitis, abnormal pigmentation, and burns to the skin. Concentrated amounts of phenol are caustic, therefore prolonged skin contact causes partial- or full-thickness burns. These burns tend to become extensive before detection, secondary to the local anesthetic properties of phenol. Ingestion of as little as 1000 mg may be fatal. Systemic effects include ventricular arrhythmias, pulmonary edema, stridor, and tachypnea. Locally, conjunctivitis, corneal edema or necrosis, and skin necrosis result.

Acute poisonings are potentially fatal, hence prompt action is necessary with copious irrigation. Polyethylene glycol (PEG; molecular weight 300 or 400 Da) has been shown to be of potential benefit, but large-volume lavage should not be delayed while PEG application is begun. Reports in the literature indicate that intravenous sodium bicarbonate may be of use to prevent some of the systemic effects of phenol.

Chromic acid causes nonpainful but corrosive ulcers upon contact with the skin. Ulceration of the nasal septum and bronchospasm can occur with inhalation. This agent causes protein coagulation. Peak blood levels are thought to be achieved within 5 hours of exposure. Symptoms may occur with just 1% total body surface area (TBSA) burn, but a 10% burn or greater is often fatal owing to its systemic effects. Irrigation is the primary treatment for exposure, but in an industrial setting, washing with a dilute solution of sodium hyposulfite or water followed by rinsing in a buffered phosphate solution may be a more specific antidote. Dimercaprol may be used at 4 mg/kg intramuscularly every 4 hours for 2 days followed by 2 to 4 mg/kg/day for 7 days in total to treat the systemic effects. Dialysis in the first 24 hours is a reasonable means to remove circulating chromium and to address existing electrolyte imbalances. Exchange transfusion may be necessary. Various ointments containing products such as 10% calcium ethylenediaminetetraacetic acid or ascorbic acid are available for small superficial burns. ^, There have been case reports supporting the early excision of chromic acid burn to assist in preventing systemic toxicity. ^,

Epichlorohydrin acid is a rare, corrosive carcinogen that is colorless and exudes a garlic-like odor. It is used in the production of glues, plastic, glycerols, and resins, as well as in paper reinforcement and water purification. It can also be converted into a binder used in the production of explosives. These burns may demonstrate a rapid progression to a full-thickness wound within hours. Management commences with copious irrigation and hemodynamic monitoring ( Fig. 33.1 ).

Epichlorohydrin acid burn 3 days after admission.

Formic acid is a strong inorganic acid used by glue makers and tanning workers. After contact, it creates an eschar, which does not prevent systemic absorption. After it is absorbed, metabolic acidosis, intravascular hemolysis with hemoglobinuria, renal failure, pulmonary complications, and abdominal pain with necrotizing pancreatitis usually occur. All patients injured by formic acid should be hospitalized because of this multitude of potential systemic effects. Formic acid is the acid most commonly used in assaults, especially in developing countries because of its easy availability.

Hydrochloric acid is one of the most commonly treated chemical burns. Hydrochloric acid and sulfuric acid are proton donors, which cause the pH in local tissues to drop to zero as hydrogen ions disassociate. Coagulation necrosis and tissue ulceration occur, leading to consolidation of connective tissue and thrombosis of intramural vessels, ulceration, fibrosis, and hemolysis. Many household cleaners contain dilute hydrochloric acid (3%–6%) and sulfuric acid and its desiccant precursor (sulfur trioxide) in concentrations up to 80% to 99%. Muriatic acid is the commercial grade of concentrated hydrochloric acid. When in contact with the skin, it denatures proteins into their chloride salts. Copious irrigation and early excision are the treatments of choice. Hydrochloric acid fumes can cause inhalation injury with acute pulmonary edema ( Figs. 33.2 and 33.3 ). Other symptoms found to occur are white or grayish discoloration of the skin and exposed mucosa. Patients may have eye, mouth, throat, and abdominal pain and injuries. They may experience hematemes is, vomiting, dizziness, headache, dyspnea, cough, tachypnea, pneumonia, laryngospasm, and ultimately respiratory failure.

Hydrochloric acid burn to the hand before blister removal.

Hydrochloric acid burn to the hand after blister removal.

Hydrofluoric acid is a corrosive that is commonly used in industrial applications and computer processing. It is used as a cleaning agent in the petroleum industry, in the production of high-octane fuel, glass etching, germicides, dyes, tanning, and fireproofing material, as well as in rust removal. Hydrofluoric acid is particularly lethal owing to its properties both as an acid and as a metabolic poison. The acid component causes coagulation necrosis and cellular death. Fluoride ions then gain a portal of entry that chelates positively charged ions such as calcium and magnesium, resulting in hypocalcemia and hypomagnesemia. This causes an efflux of intracellular calcium with resultant cell death. The fluoride ion remains active until it is completely neutralized by the bivalent cations. This may exceed the body’s ability to mobilize calcium and magnesium rapidly enough, causing muscle contraction and cellular dysfunction. Fluoride ion also acts as a metabolic poison by inhibiting Na-K ATPase, allowing efflux of potassium. Excess potassium subsequently causes shifts at nerve endings and is thought to be the cause of the extreme pain associated with hydrofluoric acid burns. Patients may present with self-limiting symptoms such as nausea; vomiting; fever; whitish tissue with surrounding erythema; immediate profound abdominal, mouth, and throat pain; skin edema; ulcers; and necrosis or stridor, laryngeal edema, wheezing, tachypnea, tetany, and potentially fatal cardiac arrhythmias.

Hydrofluoric acid burns are classified based on the concentration of the exposure. Concentrations greater than 50% cause immediate tissue destruction and pain. Concentrations of 20% to 50% result in a burn becoming apparent within several hours of exposure. Injuries from concentrations less than 20% may take up to 24 hours to become apparent.

Death from hydrofluoric acid exposure is usually secondary to systemic toxicity. Systemic symptoms are secondary to acidosis, hypocalcemia, hypomagnesemia, and hyperkalemia, which can lead to ventricular fibrillation. Thus electrolytes and cardiac rhythm should be monitored closely. When cardiac dysrhythmias develop, it is difficult to restore a normal rhythm. Compounding the problem of hypocalcemia, the fluoride ion may act as a metabolic poison in the myocardium to promote the irritability. The typical electrocardiographic change seen is QT interval prolongation. The fluoride ions can be removed by hemodialysis or cation exchange resins.

Treatments for hydrofluoric acid exposure are designed to neutralize the fluoride ion and prevent systemic toxicity. Primarily, the wound should be copiously irrigated for 30 minutes. If the concentration of exposure is less than 20% or the duration of exposure is minimal, this may serve as the extent of treatment. For more serious exposures, topical, subcutaneous, or intraarterial mixtures of calcium gluconate can be used as a first option. The topical gel is a mixture of 3.5 g of 2.5% calcium gluconate and 5 oz of water-soluble lubricant. It should be applied to the wound four to six times each day for 3 to 4 days. The mixture’s penetration into the dermis is limited by its calcium component. This is improved with the use of DMSO, which has its own associated toxicity. Calcium gluconate injections into the area of the wound (0.5 mL/cm ² of 10% calcium gluconate subcutaneously or intradermally) have also been used with good results. Intraarterial injections into the radial artery (10 mL of 10% calcium gluconate and 40 mL of 5% dextrose in water infused over 2–4 hours) can be used for management of burns to the hand, but in severe cases palmar fasciotomy may be needed. ^, This injection should be performed within 6 hours of exposure to prevent tissue necrosis and minimize pain. It should continue until the patient is symptom free.

Nitric acid is a strong oxidizing agent that can combine with organic proteins to produce organonitrates, which act as metabolic poisons. It is used in fertilizer management, casting iron and steel, and engraving. Upon skin contact, a yellow-brown stain develops on the skin and mucosa, with an eschar. Demarcation tends to occur slowly, causing difficulty in discerning burn depth. Initial treatment involves irrigation and the use of topical treatment. In addition, patients may present with whitish tinge of the teeth, eye pain, oropharyngeal pain, or abdominal pain. Patients may have dyspnea, hematemesis, dizziness, cough, tachypnea, and even develop pneumonia and laryngospasm.